As far as i know, both are PDE inhibitors. Is there any difference in terms of PDE specificity or other involved pharmacodynamic effects?
Aminophylline termination of dipyridamole stress as a trigger of coronary vasospasm in variant angina.
Picano E1, Lattanzi F, Masini M, Distante A, L'Abbate A.
Abstract
Dipyridamole testing represents an alternative to exercise stress testing for documentation of ischemia related to coronary artery disease (CAD). In such a case, ischemia is attributed to maldistribution of coronary flow during dipyridamole-induced vasodilation. The present study evaluated the potential role of dipyridamole testing in producing ischemia through a vasospastic mechanism, following rapid withdrawal of vasodilation induced by aminophylline. The possibility was tested in 36 in-hospital patients with variant angina pectoris who underwent dipyridamole infusion (up to 0.84 mg/kg over 10 minutes) with continuous 12-lead electrocardiographic and 2-dimensional echo monitoring. Medications were withdrawn from all patients. The test was pharmacologically stopped with the dipyridamole antidote (aminophylline, 80 to 240 mg intravenously over 1 to 3 minutes) in all patients. Two to 6 minutes after starting aminophylline infusion, 10 patients (28%) developed (greater than 0.10 mV) ST-segment elevation (2.9 +/- 0.8 mm from baseline), always accompanied by obvious asynergy detected by echocardiography, in the same electrocardiographic leads showing spontaneous or ergonovine-induced ST-segment elevation. Nitrates promptly resolved ischemia in all patients. At coronary angiography, 5 of these 10 patients showed significant CAD (greater than 70% lumen diameter reduction of at least 1 major coronary artery), whereas 5 had nonsignificant CAD. The rate pressure product at the onset of ST-segment elevation (after dipyridamole plus aminophylline) was considerably less than that recorded at peak exercise stress test in these patients (9,600 +/- 2,200 vs 18,400 +/- 4,900, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
http://www.ncbi.nlm.nih.gov/pubmed/3421166
Dear Mr Aldallal,
Thank you for this paper, however it seems there isn't a full version of it available. Still, this abstract offers some info. Do you suggest that aminophylline is a then a pharmacological-physiological antagonist by exerting its stronger vasodilatatory effect and thus ending the relative vasoconstrictive effect that is an effect ellicited by dipyridamole? Do you know any details behind this relative difference, even though both are PDE inhibitors?
Looking forward to answers.
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